Disease relevance of latanoprost

• Inhibition of L(p) by latanoprost was completely blocked by pertussis toxin, consistent with a G(i)-coupled mechanism [1].
• METHODS: Patients treated with latanoprost for open-angle glaucoma or ocular hypertension were randomly assigned to refill their prescriptions either at the Doheny Eye Institute clinic or a local pharmacy [2].
• CONCLUSIONS: These findings suggest that latanoprost decreases ACD in patients with glaucoma or ocular hypertension after 1 month of treatment [3].
• PURPOSE: To compare the toxicity of latanoprost and preserved and unpreserved timolol on conjunctival cells [4].
• This hyaluronic acid-induced hypertension was significantly decreased by the application of 1 drop of brimonidine (0.2%), latanoprost (0.005%), or timolol (0.5%) [5].

Psychiatry related information on latanoprost

• All groups were significantly greater that the normals but of the three it was the maximal medical therapy group (without latanoprost) that had the highest pigmentation [6].
• We evaluated the efficacy and safety of latanoprost eye drops once-weekly, compared to once-daily for improving patient compliance [7].
• Correlation between individual differences in intraocular pressure reduction and outflow facility due to latanoprost in normal-tension glaucoma patients [8].
• RESULTS: Latanoprost reduced vertigo/dysequilibrium around 30% (P < 0.05), and improved speech discrimination around 15% (P < 0.05) [9].

High impact information on latanoprost

• Inhibition of L(p) by the FP selective agonist latanoprost was additive to inhibition of vasopressin action by the EP selective agonist sulprostone [1].
• Heterologous transfection of the rabbit FPr into HEK293 cells also showed that latanoprost inhibited cAMP generation via a pertussis toxin-sensitive mechanism but did not increase cell Ca(2+) [1].
• 17-phenyl-PGF(2alpha)-IE and latanoprost caused some vasodilation in the anterior segment [10].
• MMP-9 was present after latanoprost treatment [11].
• CONCLUSIONS: The transcription of the genes for MMP-3 and -17 is increased by latanoprost treatment [11].

Chemical compound and disease context of latanoprost

• Bimatoprost treatment was associated with a higher incidence of trace-to-mild conjunctival hyperemia than latanoprost [12].
• A double-masked, randomized clinical trial comparing latanoprost with unoprostone in patients with open-angle glaucoma or ocular hypertension [13].
• A 6-week, double-masked, parallel-group study of the efficacy and safety of travoprost 0.004% compared with latanoprost 0:005%/timolol 0.5% in patients with primary open-angle glaucoma or ocular hypertension [14].
• OBJECTIVE: To study the effect of latanoprost, a prostaglandin analog, on the blood-aqueous barrier and angiographic cystoid macular edema (CME) formation in early postoperative pseudophakias [15].
• Two of the 3 studies compared latanoprost monotherapy with timolol and pilocarpine combined therapy in patients with POAG, various other glaucomas, or ocular hypertension [16].

Biological context of latanoprost

• PURPOSE: To determine whether topical treatment of mouse eyes with latanoprost alters intraocular pressure (IOP) [17].
• This study was conducted to evaluate the effect of latanoprost 0.005% on anterior chamber depth (ACD), best corrected visual acuity (BCVA), lens thickness, and anterior chamber dynamics in patients with glaucoma or ocular hypertension [3].
• Latanoprost-treated eyes showed an upregulation of MMP-3, which may be the reason for reduced extracellular matrix accumulation in such eyes [18].
• PURPOSE: To compare the short-term effects of timolol 0.5%, brimonidine 0.2%, dorzolamide 2%, and latanoprost 0.005% on intraocular pressure (IOP), blood pressure (BP), and diastolic ocular perfusion pressure (DOPP), calculated as the difference between the diastolic blood pressure (DBP) and IOP [19].
• The PGF(2alpha)- and latanoprost-acid-induced ERK1/2 activation was blocked by the presence of PKC inhibitors and downregulation of PKC by prolonged incubation with a phorbol ester [20].

Anatomical context of latanoprost

• PURPOSE: To assess the early effect of latanoprost on outflow facility and aqueous humor dynamics in the mouse [21].
• Analysis of expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases in human ciliary body after latanoprost [11].
• METHODS: Untreated and latanoprost-treated human Tenon fibroblasts were examined for the presence of MMPs and TIMPs on the mRNA and protein levels [22].
• Effects of topical latanoprost on optic nerve head circulation in rabbits, monkeys, and humans [23].
• PURPOSE: The present study was undertaken to determine whether exposure of the sclera to prostaglandin (PG)F(2alpha) or to the PGF(2alpha) analogue latanoprost acid alters mRNA for matrix metalloproteinases [24].

Associations of latanoprost with other chemical compounds

• By electron microscopy, the area of subepithelial collagen was significantly larger (P: < 0.03; Mann-Whitney test) in timolol-treated eyes (71.6%) than in control (52.7%) and latanoprost-treated eyes (57.7%) [18].
• Long-term treatment with AH13205, latanoprost, sulprostone, or bimatoprost also induces sprouting of nerve fibers [25].
• Prostaglandin analogues and mouse intraocular pressure: effects of tafluprost, latanoprost, travoprost, and unoprostone, considering 24-hour variation [26].
• PURPOSE: To determine whether latanoprost lowers IOP in prostaglandin FP receptor knockout mice [27].
• In addition, ACD was measured before and 1 hour after instillation of pilocarpine 2% at baseline and 1 month after treatment with latanoprost [3].

Gene context of latanoprost

• RESULTS: Real-time PCR results showed that 24 hours of exposure to 100 nM PGF(2alpha) significantly increased mRNA for MMP-1 and -9 (P < 0.06 Wilcoxon test) and that exposure to 100 nM latanoprost acid significantly increased mRNA for MMP-9 (P < 0.06 Wilcoxon test) [24].
• The array results also showed that latanoprost induced dose-dependent increases in the expression of TIMP-1, -2, and -3 mRNA in the scleral cultures [24].
• In NPE cells, latanoprost led to a concentration- and time-dependent increase of COX-2 mRNA levels [28].
• The levels of MMP-3 and TIMP-2 increase after treatment with latanoprost [22].
• Finally, transscleral absorption of FGF-2 was increased by up to 126% with scleral exposure to latanoprost [29].

Analytical, diagnostic and therapeutic context of latanoprost

• The drug reaches systemic concentrations that are below the level expected to stimulate FP-receptors outside the eye and it is rapidly eliminated with a half-life in plasma of 17 minutes, which explains why the clinical trials have not revealed any systemic side-effects with latanoprost [30].
• To assess the reproducibility of the ultrasonic measurements, a control group of 20 patients (20 eyes) who did not receive latanoprost was also analyzed [3].
• At 6, 12, or 24 hours after treatment, there was no difference in latanoprost- and PBS-treated eyes [17].
• CONCLUSIONS: PGF(2alpha) and latanoprost acid induce coordinated alterations of MMP gene transcription in scleral organ cultures [24].
• Latanoprost concentration in residual solution was analyzed in a masked fashion, by reversed-phase high-performance liquid chromatography (HPLC) [2].

References